This study proposes that COL4A5 deficiency may lead to HAS2 overexpression and HA accumulation to activate CD44-TGFβ signaling, thereby promoting fibrosis, encouraging further tests utilizing HAS2 and CD44 as potential therapeutic targets for XLAS patients. The gene discussed is TGFB1; the disease is X-linked hydrocephalus with stenosis of the aqueduct of Sylvius.